Dr. Jahr and I have continued to study dendrodendritic inhibition in the olfactory bulb. We have found that action potentials in the soma-dendritic exist between mitral and granule cell dendrites. This is based on the observations that IPSPs occur following spontaneous and directly evoked action potentials and also are linked to the soma-dendritic component of the antidromic action potential. This inhibitory system remains intact when propagated action potentials are blocked by tetrodotoxin. However, the system is activated only when the mitral cell reaches threshold for activating calcium spikes. Thus transmitter release from the mitral cell is not graded but is entirely dependent on activation of all-or-none calcium spikes. However, when aspartate, the putative excitatory transmitter released from mitral cells is iontophoresed into the external plexiform layer, GABA is released onto mitral cells in an entirely graded manner in the presence of tetrodotoxin. Thus the granule cell can function by releasing transmitter in the absence of spike activity. We have also been examining the effects of centrifugal transmitters on the inhibitory potentials. All of the centrifugal fibers end on the granule cell and some end on the gemmule which contains the reciprocal synapses. Norepinephrine has no effect on membrane properties of mitral cells, but it attenuates the IPSP. Enkephalin has an identical action. Glutamate, another putative centrifugal transmitter, enhances the IPSP. Thus, although the occurrence of the IPSP following a mitral cell action potential is all-or-none, the size of the IPSP can be modulated in a graded fashion. Therefore the centrifugal input to the bulb appears to exert its effect by altering the gain of the reciprocal synapse.